Black rot, caused by the soilborne fungus Ceratocystis fimbriata, is a major postharvest disease of sweetpotato (Ipomoea batatas) worldwide. Recent genomic and epidemiological studies have advanced our understanding of the interactions among host, pathogen and environment that influence disease development. Here, we review current knowledge of the pathogen's biology, epidemiology, virulence and management, and identify priorities for future research.

Zymoseptoria tritici is a significant wheat pathogen responsible for Septoria tritici blotch (STB) disease. Despite its economic impact, understanding of the molecular interactions between Z. tritici and its host remains limited, particularly the functions of many uncharacterized candidate effectors. Here, we assessed seven Z. tritici candidate effectors with elevated expression during the early biotrophic phase and transition to necrotrophy by transiently expressing them in the heterologous, non-host system Nicotiana benthamiana, with and without their predicted signal peptides. AlphaFold structural predictions revealed that two candidates share similarity with proteins of known function: a sterol-binding protein from Saccharomyces cerevisiae and a necrosis-inducing effector from Valsa mali. Effector-associated phenotypes did not always correlate with expression timing, and signal peptide presence significantly influenced observed activities. Because N. benthamiana is not a natural host of Z. tritici, observed responses may reflect conserved, host-independent activities of effectors or immune recognition by N. benthamiana, rather than their native functions in wheat. Consistent with this distinction, two candidate effectors, Mycgr3107904 and Mycgr394290, induced cell death in N. benthamiana while also modulating reactive oxygen species (ROS) burst, likely indicative of immune recognition. Some candidates attenuated ROS production, suggesting potential targeting of conserved cellular processes, whereas none suppressed PBR1-mediated cell death. Overall, our results indicate that candidate effector activities cannot be inferred from expression profiles alone, and that responses in the non-host N. benthamiana system reflect a combination of immune recognition and potential conserved activities, and primarily serve to prioritize candidates for validation in the native wheat-Z. tritici interaction.

Fusarium graminearum, the main causal agent of Fusarium head blight of wheat, secretes endoxylanases to hydrolyse xylan, a major component of hemicellulose. Mutants of the highly expressed FGSG_03624 (xylB) gene previously showed a disease severity level similar to wild-type (WT) in wheat spikes. In this study, in contrast, three independent deletion mutants of FGSG_10999 (xylA), a second highly expressed endoxylanase gene, were significantly impaired in disease severity. Surprisingly, a knock-out mutant of xylA in the ΔxylB genetic background (ΔΔxylB+A) exhibited virulence comparable to that of ΔxylB and WT. The ΔxylA mutant shared with ΔΔxylB+A a marked reduction in xylanase activity during in vitro growth, and also with ΔxylB a decreased fungal biomass and deoxynivalenol (DON) accumulation in infected spikes. In contrast to ΔΔxylB+A and ΔxylB, ΔxylA revealed down-regulation of some endoxylanase and effector genes during spike infection. In addition, when grown on a wheat spike medium, the culture filtrate of ΔxylA showed a significant reduction in total protein secretion and a more severe impairment in necrotizing activity in Nicotiana benthamiana infiltrated leaves compared with ΔxylB and ΔΔxylB+A culture filtrates. When a deletion mutant of xylB was generated in the ΔxylA genetic background, the ΔΔxylA+B mutant displayed severely reduced virulence, similar to that of the parental ΔxylA. Altogether, these results demonstrate that xylA plays a critical role in F. graminearum pathogenicity through unexpected pleiotropic, network-level alterations, as also supported by the partial restoration observed by complementing the xylA gene in ΔxylA, highlighting the strong influence of genetic background on phenotypic outcomes.

Panax notoginseng is an edible traditional medicinal plant, but it is highly susceptible to Panax notoginseng virus Y (PnVY). This study revealed that salicylic acid (SA) treatment decreases this susceptibility. The underlying molecular mechanism was elucidated by integrating physiological, multi-omics and genetic approaches. SA application alleviated PnVY-induced photosynthetic inhibition and activated antioxidant enzymes, thereby decreasing reactive oxygen species levels and maintaining redox homeostasis. Upon PnVY inoculation, SA triggered a range of defence responses. The exogenous application of SA promoted the accumulation of phenylpropanoids, alkaloids and flavonoids, which was consistent with the upregulated expression of phenylpropanoid biosynthesis-related genes. Transcriptional regulatory network analysis revealed that the ethylene-responsive transcription factor PnERF120 may positively regulate the biosynthesis of phenolic acids including SA. Overexpressing PnERF120 enhanced the resistance of P. notoginseng to PnVY, activated SA biosynthesis and signal transduction pathway, upregulated the RNA-silencing-related genes and improved phenolic acid accumulation. However, silencing PnERF120 in P. notoginseng had the opposite effect. Additionally, yeast one-hybrid and dual-luciferase assays indicated that PnERF120 binds to the promoter of PnPAL1 and activates PnPAL1 expression. In conclusion, PnERF120 positively regulates defence against PnVY infection by modulating SA biosynthesis and the SA signalling pathway.

Bacteria; Proteobacteria, gamma subdivision; Order Pseudomonadales; Family Pseudomonadaceae; Genus Pseudomonas; Pseudomonas avellanae species complex, which includes different pathogenic lineages previously classified within the P. syringae complex, namely the pathovars avellanae, theae, actinidiae, and morsprunorum race 2.

Rice foot rot, caused by Dickeya oryzae, is a destructive bacterial disease. The Vfm quorum-sensing (QS) system is a key virulence regulator of this pathogen. However, the mechanisms by which it perceives and integrates upstream environmental signals for precise transcriptional control are poorly understood. Here, we identify a cascade regulatory network involving the MarR-family transcription factors OhrR and EmrR. Deletion of ohrR in D. oryzae EC1 significantly reduced the Vfm signalling activity, diminished the production of virulence factors including phytotoxin zeamines and plant cell wall-degrading enzymes, and attenuated its pathogenicity. Molecular analyses revealed that OhrR directly bound to the key promoters in the vfm cluster (PvfmA, PvfmK, PvfmE and PvfmF) and activated their transcription. Intriguingly, OhrR also directly activated the expression of emrR, which encodes another MarR-family transcriptional regulator. In contrast to the activator role of OhrR, EmrR acted as a feedback inhibitor, directly bound to the same vfm promoter regions but repressed their transcription. OhrR-EmrR thus acts as a two-tiered 'activation-inhibition' regulatory circuit in modulation of the Vfm QS system, in which OhrR functions as a master switch for environmental signal response and initiation of the Vfm system, whereas EmrR acts as a precise brake to prevent overexpression of virulence determinants. The findings from this study unveil the fascinating interaction between OhrR-EmrR and the Vfm QS system, and depict a novel mechanism for precise virulence control in D. oryzae via complex, dynamic transcriptional reprogramming.

Botrytis cinerea triggers destructive grey mould with substantial economic losses, yet the functions of numerous pathogenicity genes remain largely unclear. Here, by screening a T-DNA insertion library, we identified BcARS2, a key component of the Microprocessor complex. BcARS2 is constitutively expressed, localizes to the nucleus, and modulates gene expression. The ΔBcars2 mutants exhibited impaired vegetative growth, enhanced conidiophore sporulation, increased conidiation, reduced sclerotial size, and increased sensitivity to multiple stresses. Pathogenicity assays showed that different inoculation methods led to distinct virulence phenotypes in ΔBcars2 mutants. Microscopic observations revealed that although the ΔBcars2 mutant formed normal appressoria and successfully invaded host cells, its invasive hyphae exhibited limited expansion. Furthermore, exogenous cAMP did not restore the impaired development of infection cushions (ICs), resulting in defective infection. Multitranscriptome analyses demonstrated that BcARS2 positively regulates BcPDI1 and BcCGF1, two key genes responsible for reactive oxygen species (ROS) homeostasis and highly expressed during the IC developmental stage. Correspondingly, deletion of BcARS2 upregulated catalase gene expression, elevated catalase activity, reduced H2O2 accumulation, disturbed ROS balance, and ultimately inhibited IC formation. In addition, most toxin biosynthesis-related genes, which are normally upregulated during IC development, were significantly downregulated in the ΔBcars2 mutant. Collectively, BcARS2 modulates the virulence of B. cinerea by regulating IC development, vegetative hyphal growth, and stress responses.

Plant-pathogenic fungi secrete small proteins, termed effectors, to reprogramme host metabolism and suppress immune responses during infection. Although transcriptional waves of effector expression have been described in several pathosystems, the cis-regulatory elements underlying their temporal coordination remain largely unknown. Here, we investigate the temporal regulation of effector genes in the biotrophic smut fungus Ustilago maydis, a model organism for fungal plant pathogenesis. By integrating transcriptome reanalysis with comparative promoter motif enrichment across biotrophic fungi, we identify distinct promoter motifs associated with defined infection phases. In U. maydis, three candidate cis-regulatory elements correlate with early, proliferative and late infection stages, respectively. Positional enrichment relative to transcription start sites supports their regulatory relevance. Functional dissection of the native pep1, stp1, and cmu1 promoters revealed strongly context-dependent contributions of these elements and synthetic promoter assays showed that the early-phase motif acts as an activating and the proliferative motif as a repressive element. Together, our findings support a combinatorial cis-regulatory code in which activating and repressive promoter elements are integrated in a promoter-specific manner to shape temporal effector expression during U. maydis infection. These elements provide a framework for engineering synthetic fungal promoters with tunable transcriptional outputs.

Sclerotinia sclerotiorum is a necrotrophic fungus that causes severe plant diseases but can also colonize wheat as a symptomless endophyte. However, the mechanism by which its effector proteins regulate this dual lifestyle remains unclear. This study aimed to identify key LysM effectors involved in S. sclerotiorum-plant interactions and elucidate their specific functions. Among seven SsLysM genes, SsLysM6 and SsLysM7 were transcriptionally upregulated during both the pathogenic infection of rapeseed and the endophytic colonization of wheat. The ΔSsLysM6 and ΔSsLysM7 mutants exhibited significantly reduced colonization abilities on both their pathogenic host (rapeseed) and their endophytic host (wheat). Transient expression of SsLysM6 and SsLysM7 in Nicotiana benthamiana leaves demonstrated that both effectors suppress chitin-induced immune responses, including reactive oxygen species (ROS) bursts, MAPK activation, and immune gene expression. Recombinant SsLysM6 and SsLysM7 proteins exhibited chitin-binding ability and efficiently suppressed chitin-triggered ROS bursts in wheat leaves. These findings provide critical insights into the molecular mechanism by which S. sclerotiorum establishes compatible interactions across genetically diverse hosts, highlight the central role of LysM effectors in fungal adaptation to distinct lifestyles, and offer new perspectives on the evolutionary continuum between pathogenic and endophytic fungi.

Green mould is one of the major postharvest diseases affecting citrus. Although evidence indicates that microRNAs (miRNAs) participate in plant defence responses, their roles and regulatory mechanisms in citrus resistance to green mould remain unclear. Small RNA sequencing identified several defence-associated miRNAs involved in citrus resistance to Penicillium digitatum. Among them, transient overexpression screening identified Csi-miR3954b as the most effective miRNA, reducing disease incidence by 24.4% compared with the control at 5 days post-inoculation (dpi). Subsequent transient overexpression and short tandem target mimic (STTM)-mediated suppression assays demonstrated that Csi-miR3954b positively regulates citrus resistance to green mould, with transient overexpression reducing disease incidence by 22.7% and STTM-mediated suppression increasing it by 9.6% at 5 dpi. Degradome sequencing, transient assays in Nicotiana benthamiana leaves and expression analysis identified CsCE70 and CsPLA1 as the direct targets of Csi-miR3954b. Transcriptome analysis showed that CsCE70 and CsPLA1 mainly regulated phenolic acid and flavonoid biosynthesis, respectively. Transient overexpression of CsCE70 and CsPLA1 increased disease incidence by 17.4% and 10.4%, respectively, compared with the control at 5 dpi, suggesting that both genes negatively regulated citrus resistance to P. digitatum. Silencing these genes enhanced its resistance, accompanied by the accumulation of phenolics and flavonoids in the peel. In general, the results showed that the Csi-miR3954b-CsCE70/CsPLA1 regulatory modules enhanced citrus resistance to P. digitatum by promoting the biosynthesis of phenolic acids and flavonoids. These results provide new insights into miRNA-mediated postharvest disease resistance and potential molecular strategies for improving citrus postharvest protection.

Viral infection often induces chlorosis, a symptom closely associated with chlorophyll (Chl) degradation. STAY-GREEN (SGR) proteins are key regulators of Chl breakdown, but their roles in plant virus resistance remain poorly understood. In this study, we identified six NtSGR family genes in Nicotiana tabacum and functionally characterized NtSGRL1 during tomato yellow leaf curl virus (TYLCV) infection. TYLCV drastically upregulates NtSGRL1 (149-fold at 4 days post-inoculation [dpi] vs. control), suggesting its involvement in the tobacco-TYLCV interaction. Subcellular localization revealed that NtSGRL1 is targeted to both the nucleus and chloroplast, and yeast assays confirmed its transcriptional activation activity, indicating potential dual functions. TYLCV accumulation was reduced by 1995-fold in Ntsgrl1 mutants relative to wild-type (WT) plants at 10 dpi. Further assays with tomato spotted wilt virus (TSWV), potato virus Y (PVY) and tobacco mosaic virus (TMV) showed that viral accumulation in Ntsgrl1 mutants was reduced by 62%-99%, suggesting that NtSGRL1 may affect resistance to additional tested viruses. Transcriptomics revealed 1470 differentially expressed genes in TYLCV-infected Ntsgrl1 plants enriched in MAPK signalling and phenylpropanoid biosynthesis pathways. Virus-induced gene silencing (VIGS)-based validation further supported the involvement of these pathways in TYLCV resistance. Overall, this study identifies NtSGRL1 as a critical regulator of antiviral resistance in tobacco and reveals its dual functional roles as both a Chl-related enzyme and a transcriptional regulator. These findings provide new insights into plant antiviral mechanisms and potential genetic resources for breeding virus-resistant crops.

The complete genome sequence of a relatively weak virulent tobacco pathogen, Pseudomonas syringae pv. tabaci 8018 (Pta8018) was determined to elucidate key genetic elements that cause disease. Genome comparison of Pta8018 to the previously available P. syringae pv. tabaci strains revealed that Pta8018 and Pta11528 had high genome synteny, with an approximately 5 Mb chromosome inversion in Pta6605. Furthermore, Pta8018 had lost the pathogenicity island GI-1 including a tabtoxin biosynthesis gene cluster and showed weak virulence on Nicotiana tabacum 'Xanthi NC' (Xanthi). When inoculated into several tobacco cultivars, Pta8018 caused leaf angular spot not only in Xanthi but also in N. tabacum cultivars Burley21 and N509, while Pta6605 did not cause disease in Burley21 and N509 due to the presence of avirulence factor HopAZ1. We found that a mutation in hopAZ1 allows Pta8018 to avoid recognition in these cultivars. Introduction of intact hopAZ1 of Pta6605 into Pta8018 rendered it avirulent to N509 and Burley21, revealing that effector HopAZ1 is a key virulence determinant of P. syringae pv. tabaci. Our data show that although Pta8018 has reduced virulence strength by the loss of GI-1 in Xanthi, it expanded its host range to two other cultivars through mutation of hopAZ1.

Pine wilt disease (PWD), caused by the pine wood nematode (PWN, Bursaphelenchus xylophilus), poses a severe threat to global pine forests. Plants can enhance their resistance to external stresses by eliciting secondary metabolites; however, the transcriptional regulatory mechanisms governing this defence response in pines remain largely unexplored. Here, we report a novel defence regulatory module in Pinus massoniana. PmWRKY-10 may participate in PWN resistance by regulating the biosynthesis of the nematicidal metabolite pinosylvin monomethyl ether (PME). We first demonstrated that PME accumulation is closely linked to resistance in P. massoniana and provided evidence that PME exhibits direct and potent nematicidal activity against PWN in vitro. By integrating multi-omics profiling with weighted gene co-expression network analysis (WGCNA), we identified PmPMT2-1 as a key candidate associated with PME biosynthesis and accumulation, while recognizing that it is unlikely to function as the sole rate-limiting determinant. Functional analyses demonstrated that PmPMT2-1 overexpression promoted PME accumulation and enhanced resistance, whereas silencing the gene impaired both processes. Mechanistically, we identified PmWRKY-10 as an upstream transcriptional activator that directly binds to the W-box element in the PmPMT2-1 promoter, inducing its transcription. Our work delineates a complete PmWRKY-10→PmPMT2-1→PME transcriptional-metabolic pathway that is essential for stilbene-based resistance in pine. This discovery not only provides fundamental insights into the inducible defence mechanisms of conifers but also identifies key genetic targets for breeding resistant varieties and developing sustainable forest management strategies.

Southern corn rust (SCR), caused by the biotrophic fungus Puccinia polysora, severely threatens maize yield worldwide. In this study, we identified ZmJAZ12, a member of the JASMONATE ZIM-domain (JAZ) protein family, as a negative regulator of SCR resistance in maize. Genome-wide association study (GWAS) and expression analyses revealed that the expression level of ZmJAZ12 was negatively correlated with SCR resistance, and the resistant haplotypes exhibited significantly lower transcript abundance of ZmJAZ12. The ZmJAZ12 overexpression (OE) lines showed enhanced susceptibility to SCR, while ZmJAZ12 knockout mutants generated via CRISPR/Cas9-mediated gene editing were more resistant to SCR. Transcriptomic profiling revealed that downregulation of key genes in the salicylic acid (SA) and jasmonic acid (JA) pathways occurred in the OE lines. ZmJAZ12 interacted with ZmMYC5, a core transcription factor in the JA signalling cascade, forming a regulatory module that regulates hormonal signalling and immune responses. Collectively, these findings reveal that ZmJAZ12 acts as a susceptibility gene, providing evidence for the JA/SA signalling crosstalk mechanism in plant immunity. This study provides a potential genetic target for enhancing disease resistance in maize breeding.

RNA viruses usually reprogramme host cellular lipid metabolism to create favourable replication microenvironments, yet the broader biological significance of these lipid changes is largely unknown. To explore the potential roles of virus-induced lipids, we employed an economically important plant pathogen cucumber mosaic virus (CMV), which has a single-stranded, positive-sense, tripartite RNA genome replicating in host tonoplasts. Lipidomic analysis of purified tonoplasts revealed that CMV infection increased the relative accumulation of sphingolipids in tonoplasts. This is consistent with the increased expression levels of these enzymes involved in sphingolipid biosynthesis, particularly 3-ketosphinganine reductase (TSC10). Virus-induced silencing of Nb-TSC10 in Nicotiana benthamiana impaired CMV replication by triggering the unfolded protein response (UPR). Furthermore, we found that salicylic acid (SA) serves as a central regulator of UPR-mediated antiviral immunity. Notably, a specific sphingolipid, ceramide, was found to alleviate the UPR, suggesting an important role for sphingolipids during CMV infection: CMV subverts SA-induced immunity by rewiring sphingolipid biosynthesis to inhibit the UPR-mediated defence. This work advances mechanistic understanding of viral counterdefence strategies through sphingolipid-mediated modulation of UPR during plant-pathogen interactions.